Gut ischemia/reperfusion produces lung injury independent of endotoxin
作者:
KAORU KOIKE,
ERNEST MOORE,
FREDERICK MOORE,
ROBERT READ,
VIRGINIA CARL,
ANIRBAN BANERJEE,
期刊:
Critical Care Medicine
(OVID Available online 1994)
卷期:
Volume 22,
issue 9
页码: 1438-1444
ISSN:0090-3493
年代: 1994
出版商: OVID
关键词: intestines, small;superoxides;reactive oxygen species;lipopolysaccharide;neutrophils;translocation, bacterial;permeability;multiple organ failure;adult respiratory distress syndrome;critical illness
数据来源: OVID
摘要:
ObjectiveBacterial translocation from the gut has been invoked as a common inciting event for postinjury multiple organ failure. We previously showed that gut ischemia/reperfusion induces remote organ injury. The purpose of this study was to ascertain if endotoxin has a pivotal mechanistic role in this process.DesignProspective, randomized study.SettingAnimal laboratory.SubjectsSprague-Dawley rats weighing 300 to 350 g.InterventionsAnesthetized animals underwent 45 mins of superior mesenteric artery occlusion and 2 hrs of reperfusion; sham laparotomy served as controls. Endotoxin was eliminated with the murine immunoglobulin (Ig) M antibody E5, 3 mg/kg iv before the study.Measurements and Main ResultsPlasma endotoxin was measured by the limulus amebocyte lysate assay. At 2 hrs of reperfusion, circulating neutrophil priming was determined by the difference in superoxide generation with and without the activating stimulus, N-formyl-Met-Leu-Phe. Neutrophil sequestration in the lung was quantitated by myeloperoxidase activity, and by lung endothelial permeability by125I albumin lung/blood ratio. Endotoxin concentrations were not significantly (significance determined asp< .05) different between the gut ischemia/reperfusion and laparotomy groups (n = ≥5) during ischemia or reperfusion. Circulating neutrophil priming, neutrophil accumulation in the lung, and lung injury were provoked by gut ischemia/reperfusion, but not altered by endotoxin elimination.ConclusionGut ischemia/reperfusion primes circulating neutrophils and produces lung injury by a mechanism independent of endotoxin. (Crit Care Med 1994; 22:1438–1444)
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